O-GlcNAcylation and stablization of SIRT7 promote pancreatic cancer progression by blocking the SIRT7-REGγ interaction
Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal cancers and its dismal prognosis indicates the urgent need to elucidate the potential oncogenic mechanisms. SIRT7 is a classic NAD + -dependent deacetylase that stabilizes the transformed state of cancer cells. However, its functional...
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| Veröffentlicht in: | Cell death and differentiation 2022-10, Vol.29 (10), p.1970-1981 |
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| creator | He, Xiaoman Li, Yongzhou Chen, Qing Zheng, Lei Lou, Jianyao Lin, Chuanshuai Gong, Jiali Zhu, Yi Wu, Yulian |
| description | Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal cancers and its dismal prognosis indicates the urgent need to elucidate the potential oncogenic mechanisms. SIRT7 is a classic NAD
+
-dependent deacetylase that stabilizes the transformed state of cancer cells. However, its functional roles in PDAC are still unclear. Here, we found that SIRT7 expression is upregulated and predicts poor prognosis in PDAC. Then we screened the new interacting proteins of SIRT7 by mass spectrometry and the results showed that SIRT7 can interact with O-GlcNAc transferase (OGT). O-GlcNAcylation stabilizes the SIRT7 protein by inhibiting its interaction with REGγ to prevent degradation, and hyper-O-GlcNAcylation in pancreatic cancer cells leads to hypoacetylation of H3K18 via SIRT7, which promotes transcriptional repression of several tumour suppressor genes. In addition, SIRT7 O-GlcNAcylation at the serine 136 residue (S136) is required to maintain its protein stability and deacetylation ability. In vivo and in vitro experiments showed that blocking SIRT7 O-GlcNAcylation at S136 attenuates tumour progression. Collectively, we demonstrate that O-GlcNAcylation is an important post-translational modification of SIRT7 in pancreatic cancer cells, and elucidating this mechanism of SIRT7 is expected to pave the way for the development of novel therapeutic methods in the future. |
| doi_str_mv | 10.1038/s41418-022-00984-3 |
| format | Article |
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-dependent deacetylase that stabilizes the transformed state of cancer cells. However, its functional roles in PDAC are still unclear. Here, we found that SIRT7 expression is upregulated and predicts poor prognosis in PDAC. Then we screened the new interacting proteins of SIRT7 by mass spectrometry and the results showed that SIRT7 can interact with O-GlcNAc transferase (OGT). O-GlcNAcylation stabilizes the SIRT7 protein by inhibiting its interaction with REGγ to prevent degradation, and hyper-O-GlcNAcylation in pancreatic cancer cells leads to hypoacetylation of H3K18 via SIRT7, which promotes transcriptional repression of several tumour suppressor genes. In addition, SIRT7 O-GlcNAcylation at the serine 136 residue (S136) is required to maintain its protein stability and deacetylation ability. In vivo and in vitro experiments showed that blocking SIRT7 O-GlcNAcylation at S136 attenuates tumour progression. Collectively, we demonstrate that O-GlcNAcylation is an important post-translational modification of SIRT7 in pancreatic cancer cells, and elucidating this mechanism of SIRT7 is expected to pave the way for the development of novel therapeutic methods in the future.</description><identifier>ISSN: 1350-9047</identifier><identifier>EISSN: 1476-5403</identifier><identifier>DOI: 10.1038/s41418-022-00984-3</identifier><identifier>PMID: 35422493</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>101/58 ; 13/89 ; 631/67/395 ; 631/80/221 ; Adenocarcinoma ; Apoptosis ; Autoantigens ; Biochemistry ; Biomedical and Life Sciences ; Carcinoma, Pancreatic Ductal ; Cell Biology ; Cell Cycle Analysis ; Cell Proliferation ; Deacetylation ; Gene silencing ; Humans ; Life Sciences ; Mass spectroscopy ; N-Acetylglucosaminyltransferases - genetics ; N-Acetylglucosaminyltransferases - metabolism ; NAD - metabolism ; O-GlcNAcylation ; Pancreatic cancer ; Pancreatic Neoplasms ; Pancreatic Neoplasms - metabolism ; Post-translation ; Prognosis ; Proteasome Endopeptidase Complex ; Protein Processing, Post-Translational ; Serine - metabolism ; Sirtuins - genetics ; Sirtuins - metabolism ; Stem Cells ; Tumor suppressor genes ; Tumors</subject><ispartof>Cell death and differentiation, 2022-10, Vol.29 (10), p.1970-1981</ispartof><rights>The Author(s) 2022</rights><rights>2022. The Author(s).</rights><rights>The Author(s) 2022. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c474t-80325275102e1d3862e7db720d8014c0610c8fe8550bfc7943e5827e1a58d27f3</citedby><cites>FETCH-LOGICAL-c474t-80325275102e1d3862e7db720d8014c0610c8fe8550bfc7943e5827e1a58d27f3</cites><orcidid>0000-0002-2199-4353 ; 0000-0002-1459-0158 ; 0000-0001-6179-4586 ; 0000-0002-9416-6663 ; 0000-0003-2675-5834 ; 0000-0001-6662-9440 ; 0000-0002-6576-8008 ; 0000-0002-4090-0551 ; 0000-0003-0548-2742</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9525610/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9525610/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,41464,42533,51294,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35422493$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>He, Xiaoman</creatorcontrib><creatorcontrib>Li, Yongzhou</creatorcontrib><creatorcontrib>Chen, Qing</creatorcontrib><creatorcontrib>Zheng, Lei</creatorcontrib><creatorcontrib>Lou, Jianyao</creatorcontrib><creatorcontrib>Lin, Chuanshuai</creatorcontrib><creatorcontrib>Gong, Jiali</creatorcontrib><creatorcontrib>Zhu, Yi</creatorcontrib><creatorcontrib>Wu, Yulian</creatorcontrib><title>O-GlcNAcylation and stablization of SIRT7 promote pancreatic cancer progression by blocking the SIRT7-REGγ interaction</title><title>Cell death and differentiation</title><addtitle>Cell Death Differ</addtitle><addtitle>Cell Death Differ</addtitle><description>Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal cancers and its dismal prognosis indicates the urgent need to elucidate the potential oncogenic mechanisms. SIRT7 is a classic NAD
+
-dependent deacetylase that stabilizes the transformed state of cancer cells. However, its functional roles in PDAC are still unclear. Here, we found that SIRT7 expression is upregulated and predicts poor prognosis in PDAC. Then we screened the new interacting proteins of SIRT7 by mass spectrometry and the results showed that SIRT7 can interact with O-GlcNAc transferase (OGT). O-GlcNAcylation stabilizes the SIRT7 protein by inhibiting its interaction with REGγ to prevent degradation, and hyper-O-GlcNAcylation in pancreatic cancer cells leads to hypoacetylation of H3K18 via SIRT7, which promotes transcriptional repression of several tumour suppressor genes. In addition, SIRT7 O-GlcNAcylation at the serine 136 residue (S136) is required to maintain its protein stability and deacetylation ability. In vivo and in vitro experiments showed that blocking SIRT7 O-GlcNAcylation at S136 attenuates tumour progression. Collectively, we demonstrate that O-GlcNAcylation is an important post-translational modification of SIRT7 in pancreatic cancer cells, and elucidating this mechanism of SIRT7 is expected to pave the way for the development of novel therapeutic methods in the future.</description><subject>101/58</subject><subject>13/89</subject><subject>631/67/395</subject><subject>631/80/221</subject><subject>Adenocarcinoma</subject><subject>Apoptosis</subject><subject>Autoantigens</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Carcinoma, Pancreatic Ductal</subject><subject>Cell Biology</subject><subject>Cell Cycle Analysis</subject><subject>Cell Proliferation</subject><subject>Deacetylation</subject><subject>Gene silencing</subject><subject>Humans</subject><subject>Life Sciences</subject><subject>Mass spectroscopy</subject><subject>N-Acetylglucosaminyltransferases - genetics</subject><subject>N-Acetylglucosaminyltransferases - metabolism</subject><subject>NAD - 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genetics</topic><topic>N-Acetylglucosaminyltransferases - metabolism</topic><topic>NAD - metabolism</topic><topic>O-GlcNAcylation</topic><topic>Pancreatic cancer</topic><topic>Pancreatic Neoplasms</topic><topic>Pancreatic Neoplasms - metabolism</topic><topic>Post-translation</topic><topic>Prognosis</topic><topic>Proteasome Endopeptidase Complex</topic><topic>Protein Processing, Post-Translational</topic><topic>Serine - metabolism</topic><topic>Sirtuins - genetics</topic><topic>Sirtuins - metabolism</topic><topic>Stem Cells</topic><topic>Tumor suppressor genes</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>He, Xiaoman</creatorcontrib><creatorcontrib>Li, Yongzhou</creatorcontrib><creatorcontrib>Chen, Qing</creatorcontrib><creatorcontrib>Zheng, Lei</creatorcontrib><creatorcontrib>Lou, Jianyao</creatorcontrib><creatorcontrib>Lin, Chuanshuai</creatorcontrib><creatorcontrib>Gong, Jiali</creatorcontrib><creatorcontrib>Zhu, Yi</creatorcontrib><creatorcontrib>Wu, Yulian</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest Central (New)</collection><collection>ProQuest One Academic (New)</collection><collection>ProQuest Health & Medical Research Collection</collection><collection>ProQuest One Academic Middle East (New)</collection><collection>ProQuest One Health & Nursing</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Applied & Life Sciences</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cell death and differentiation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>He, Xiaoman</au><au>Li, Yongzhou</au><au>Chen, Qing</au><au>Zheng, Lei</au><au>Lou, Jianyao</au><au>Lin, Chuanshuai</au><au>Gong, Jiali</au><au>Zhu, Yi</au><au>Wu, Yulian</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>O-GlcNAcylation and stablization of SIRT7 promote pancreatic cancer progression by blocking the SIRT7-REGγ interaction</atitle><jtitle>Cell death and differentiation</jtitle><stitle>Cell Death Differ</stitle><addtitle>Cell Death Differ</addtitle><date>2022-10-01</date><risdate>2022</risdate><volume>29</volume><issue>10</issue><spage>1970</spage><epage>1981</epage><pages>1970-1981</pages><issn>1350-9047</issn><eissn>1476-5403</eissn><abstract>Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal cancers and its dismal prognosis indicates the urgent need to elucidate the potential oncogenic mechanisms. SIRT7 is a classic NAD
+
-dependent deacetylase that stabilizes the transformed state of cancer cells. However, its functional roles in PDAC are still unclear. Here, we found that SIRT7 expression is upregulated and predicts poor prognosis in PDAC. Then we screened the new interacting proteins of SIRT7 by mass spectrometry and the results showed that SIRT7 can interact with O-GlcNAc transferase (OGT). O-GlcNAcylation stabilizes the SIRT7 protein by inhibiting its interaction with REGγ to prevent degradation, and hyper-O-GlcNAcylation in pancreatic cancer cells leads to hypoacetylation of H3K18 via SIRT7, which promotes transcriptional repression of several tumour suppressor genes. In addition, SIRT7 O-GlcNAcylation at the serine 136 residue (S136) is required to maintain its protein stability and deacetylation ability. In vivo and in vitro experiments showed that blocking SIRT7 O-GlcNAcylation at S136 attenuates tumour progression. Collectively, we demonstrate that O-GlcNAcylation is an important post-translational modification of SIRT7 in pancreatic cancer cells, and elucidating this mechanism of SIRT7 is expected to pave the way for the development of novel therapeutic methods in the future.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>35422493</pmid><doi>10.1038/s41418-022-00984-3</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-2199-4353</orcidid><orcidid>https://orcid.org/0000-0002-1459-0158</orcidid><orcidid>https://orcid.org/0000-0001-6179-4586</orcidid><orcidid>https://orcid.org/0000-0002-9416-6663</orcidid><orcidid>https://orcid.org/0000-0003-2675-5834</orcidid><orcidid>https://orcid.org/0000-0001-6662-9440</orcidid><orcidid>https://orcid.org/0000-0002-6576-8008</orcidid><orcidid>https://orcid.org/0000-0002-4090-0551</orcidid><orcidid>https://orcid.org/0000-0003-0548-2742</orcidid><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Springer Nature - Complete Springer Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | 101/58 13/89 631/67/395 631/80/221 Adenocarcinoma Apoptosis Autoantigens Biochemistry Biomedical and Life Sciences Carcinoma, Pancreatic Ductal Cell Biology Cell Cycle Analysis Cell Proliferation Deacetylation Gene silencing Humans Life Sciences Mass spectroscopy N-Acetylglucosaminyltransferases - genetics N-Acetylglucosaminyltransferases - metabolism NAD - metabolism O-GlcNAcylation Pancreatic cancer Pancreatic Neoplasms Pancreatic Neoplasms - metabolism Post-translation Prognosis Proteasome Endopeptidase Complex Protein Processing, Post-Translational Serine - metabolism Sirtuins - genetics Sirtuins - metabolism Stem Cells Tumor suppressor genes Tumors |
| title | O-GlcNAcylation and stablization of SIRT7 promote pancreatic cancer progression by blocking the SIRT7-REGγ interaction |
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